DOI:10.2214/AJR.04.0918
AJR 2006; 187:W33-W41
© American Roentgen Ray Society
Sonography of Budd-Chiari Syndrome
Xavier Bargalló1,
Rosa Gilabert1,
Carlos Nicolau1,
Juan Carlos García-Pagán1,
Juan Ramón Ayuso1 and
Concepció Brú1
1 All authors: Department of Radiology, Hospital Clinic, C/Villarroel, 170,
Barcelona, Spain 08036.
Received June 10, 2004;
accepted after revision April 6, 2005.
Address correspondence to X. Bargalló.
WEB
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Abstract
OBJECTIVE. The purpose of this pictorial essay is to review the
color Doppler sonographic features of Budd-Chari syndrome.
CONCLUSION. Combining color and spectral data, sonography provides
hemodynamic and anatomic information about vessel patency and collateral
vessel formation. The diagnosis of Budd-Chari syndrome is based on the
involvement of hepatic veins although intrahepatic collateral circulation and
dilated caudate veins are also important and frequent signs. Half of the
patients will develop regenerative nodules that can simulate hepatocellular
carcinoma.
Keywords: Budd-Chiari syndrome • liver • sonography
Introduction
Budd-Chiari syndrome is the manifestation of a hepatic venous outflow
obstruction, which can be located anywhere above the level of the hepatic
venules. In Western countries, Budd-Chiari syndrome is the result of a
prothrombotic disorder (> 75% of patients), whereas membranous obstruction
of the inferior vena cava is the cause of most cases in Asia
[1,
2].
Young women are predominantly affected. Clinical presentation varies from a
fulminant form with severe portal hypertension; acute or subacute forms
(abdominal pain, ascites, and different degrees of liver failure); chronic
forms (the more frequent); to an asymptomatic condition. However, this
classification does not provide enough information to establish prognostic or
therapeutic criteria. The clinical correlation depends on both the extent of
the obstructive process and how quickly it develops. Treatment includes
anticoagulation therapy, management of portal hypertension complications,
liver decompression (transjugular intrahepatic portosystemic shunt [TIPS] or
surgical portosystemic shunt), and liver transplantation. Patients surviving
for 2 years after diagnosis have a good prognosis
[1].
X-ray venography has been the reference study in providing direct evidence
of hepatic vein thrombosis and collateral vessel formation. However, color
Doppler sonography offers noninvasive hemodynamic and anatomic information
about hepatic and portal vein patency and collateral vessel formation
[1-4].
When diagnosing Budd-Chiari syndrome, there are different categories of
signs. The first category is specific signs such as evidence of hepatic vein
involvement (e.g., nonvisualization, fibrous cord, thrombosis, and stenosis).
The second category is suggestive signs such as evidence of intrahepatic
collateral circulation (e.g., spiderweb collaterals, subcapsular vessels,
arcuate vessels to the inferior vena cava, collaterals between portal and
venous hepatic systems) and a caudate vein that is 3 mm or larger. The third
category is other findings and is composed of findings that are shared with
other conditions such as benign regenerative nodules, caudate lobe
hypertrophia, nonhomogeneous parenchymal structure, portal thrombosis,
recanalized umbilical vein, and ascites.
Hepatic Vein Involvement
Findings that suggest hepatic vein involvement are nonvisualization of the
vein on Doppler color sonography (Figs.
1A,
1B,
2A,
2B,
2C,
2D,
3A, and
3B); a fibrous cord replacing
the vein (Figs. 1A,
1B,
2A,
2B,
2C, and
2D); thrombus filling the
lumen, which may be seen in acute forms of Budd-Chiari syndrome but is not
common (Figs. 4A,
4B,
5A,
5B, and
5C); and stenosis (Figs.
6A and
6B).
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Fig. 1A —45-year-old woman with 1-month history of weakness and
enlargement of abdominal diameter. Gray-scale sonogram obtained in right
subcostal plane shows echogenic bands replacing right and left hepatic veins
(open arrowheads) and failed to show middle hepatic vein. Liver
parenchyma is heterogeneous with large central hypoechoic area
(arrows) representing edema caused by congestion. Note perihepatic
ascites. Transjugular intrahepatic portosystemic shunt (TIPS) placement was
mandatory. This case illustrates acute Budd-Chiari syndrome with obstruction
of three major hepatic veins combining signs related to hepatic vein
obstruction and those related to portal hypertension (liver edema and
ascites). However, presence of fibrous cords replacing veins in this acute
setting would support endophlebitis as pathogenic factor.
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Fig. 1B —45-year-old woman with 1-month history of weakness and
enlargement of abdominal diameter. Color Doppler sonogram obtained in right
subcostal plane 1 year later shows capsular hypertrophied vessels (open
arrowheads).
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Fig. 2A —40-year-old woman with subacute Budd-Chiari syndrome (2
months since onset of symptoms) presenting as thrombosis of right and middle
hepatic veins. Transverse Doppler sonogram shows lack of visualization of
distal part of middle hepatic vein. Segment near inferior vena cava is
filiform (open arrowheads) and has no flow. Irregular pulsed Doppler
signals that are obtained represent artifactual transmission of cardiac
contraction.
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Fig. 2B —40-year-old woman with subacute Budd-Chiari syndrome (2
months since onset of symptoms) presenting as thrombosis of right and middle
hepatic veins. Gray-scale sonogram obtained 1 year later shows fibrous cords
replacing hepatic veins (open arrowheads). ivc = inferior vena
cava.
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Fig. 2C —40-year-old woman with subacute Budd-Chiari syndrome (2
months since onset of symptoms) presenting as thrombosis of right and middle
hepatic veins. Color Doppler sonogram (C) and pulsed Doppler sonogram
(D) display spontaneous direct portacaval shunt (arrow)
between right portal vein (rpv) and inferior vena cava (ivc). This spontaneous
shunt was by itself unable to provide enough hepatic decompression, and
transjugular intrahepatic portosystemic shunt (TIPS) placement was necessary.
Note that spectral Doppler waveform in D shows noncontinuous flow.
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Fig. 2D —40-year-old woman with subacute Budd-Chiari syndrome (2
months since onset of symptoms) presenting as thrombosis of right and middle
hepatic veins. Color Doppler sonogram (C) and pulsed Doppler sonogram
(D) display spontaneous direct portacaval shunt (arrow)
between right portal vein (rpv) and inferior vena cava (ivc). This spontaneous
shunt was by itself unable to provide enough hepatic decompression, and
transjugular intrahepatic portosystemic shunt (TIPS) placement was necessary.
Note that spectral Doppler waveform in D shows noncontinuous flow.
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Fig. 3A —35-year-old woman. At time of Budd-Chiari syndrome diagnosis,
patient had 1-year history of mild symptoms (unspecific abdominal pain).
Patient developed important collateral circulation in follow-up. Color Doppler
sonogram obtained in intercostal plane displays attempt to replace obstructed
right hepatic vein by means of fragmented, little veins (open
arrowheads), which follow same track as that of previous occluded
vein.
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Fig. 3B —35-year-old woman. At time of Budd-Chiari syndrome diagnosis,
patient had 1-year history of mild symptoms (unspecific abdominal pain).
Patient developed important collateral circulation in follow-up. Color Doppler
sonogram obtained in intercostal plane shows spontaneous portacaval shunt. ivc
= inferior vena cava.
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Fig. 4A —50-year-old woman with 2-month history of refractory ascites.
Color Doppler sonogram obtained in intercostal plane shows uncolored right
hepatic vein (open arrowheads) that is occupied by fine echoes
thought to be related to acute thrombosis. Fine perivenous vessels
(arrows) represent incipient collateral circulation.
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Fig. 4B —50-year-old woman with 2-month history of refractory ascites.
Color Doppler sonogram obtained in intercostal plane shows large tortuous
subcapsular vein going to drain to inferior vena cava (open
arrowheads). Hypertrophied subcapsular veins may shunt blood from liver
to systemic veins (azygos vein, intercostal veins) or directly to inferior
vena cava creating new intrahepatic and extrahepatic circulation.
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Fig. 5A —50-year-old man with secondary Budd-Chiari syndrome. Tumoral
invasion of hepatic veins may be seen in hepatocellular carcinoma and other
invasive tumors such as sarcoma. Extended hepatocarcinoma tends to invade
vascular structures, although isolated invasion of hepatic vein does not have
clinical correlation. Gray-scale sonogram obtained in intercostal plane shows
large tumor (arrows) with central anechoic area (arrowheads)
that represents necrosis. Histologic study diagnosed paraganglioma.
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Fig. 5B —50-year-old man with secondary Budd-Chiari syndrome. Tumoral
invasion of hepatic veins may be seen in hepatocellular carcinoma and other
invasive tumors such as sarcoma. Extended hepatocarcinoma tends to invade
vascular structures, although isolated invasion of hepatic vein does not have
clinical correlation. Gray-scale sonogram obtained in right subcostal plane
shows tumor invading middle hepatic vein (mhv). Thin arrows show vein
invasion. Note presence of small vessels (thick arrows) going toward
patent left hepatic vein (lhv). In this case, patient shows no symptoms
associated with vascular infiltration.
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Fig. 5C —50-year-old man with secondary Budd-Chiari syndrome. Tumoral
invasion of hepatic veins may be seen in hepatocellular carcinoma and other
invasive tumors such as sarcoma. Extended hepatocarcinoma tends to invade
vascular structures, although isolated invasion of hepatic vein does not have
clinical correlation. Color Doppler sonogram in right subcostal plane shows
small vessels in blue (arrows) going from middle hepatic vein (mhv)
to left hepatic vein (lhv). Note aliasing in middle hepatic vein caused by
proximal obstruction. ivc = inferior vena cava.
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Fig. 6A —59-year-old woman with orthotopic liver transplantation for
chronic hepatitis C virus. Color Doppler sonogram obtained in right
intercostal plane shows right hepatic vein (rhv) with inverted flow
(red). mhv = middle hepatic vein.
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Fig. 6B —59-year-old woman with orthotopic liver transplantation for
chronic hepatitis C virus. Color Doppler sonogram slightly tilted relative to
previous image shows right hepatic vein (out of plane) draining through
collateral vessel (arrowhead) to middle hepatic vein (mhv), resulting
in presence of "bicolored" hepatic vein. Collateral vessel
connecting occluded (or stenotic) hepatic vein to neighboring patent hepatic
vein (blue) results in presence of "bicolored" hepatic
veins. Thus, "bicolored" phenomenon consists of flow, which turns
away and toward transducer in same vessel. In this case, it was incidental
finding that was thought to be related to stenosis of hepatic vein because
junction with vena cava was not clearly depicted.
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The presence of at least one of these specific signs makes the radiologic
diagnosis of Budd-Chiari syndrome, but this finding does not always have a
clinical correlation. Occlusion of a single vein is usually clinically silent,
but two or three main hepatic veins can be occluded without significant
symptoms [5]. This fact may be
explained by a step-by-step occlusion of one followed by two or more veins
with simultaneous development of venous collaterals. This hypothesis is
supported by the finding of different degrees of involvement at the hepatic
veins on color Doppler sonography.
The role of thrombosis as a leading cause of obstruction is unclear. In
explanted livers, it is more common to find fibrous subendothelial thickening
related to primary endophlebitis, accounting for the nonvisualization of the
vein or the fibrous cord transformation
[1,
2].
Isolated abnormalities in the hepatic waveform morphology, such as absence
of phasic oscillations resulting in a flat flow, are of limited value in the
diagnosis unless they are associated with intrahepatic collateral vessels
because a similar Doppler pattern can be observed in patients with fatty
liver, active chronic hepatitis, or liver cirrhosis.
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Fig. 7A —55-year-old man with paroxysmal nocturnal hemoglobinuria
(PNH) who presented with 6-week history of generalized edema and diffuse
abdominal pain. Sonographic study was performed showing that right and left
hepatic veins were obstructed. Term "spiderweb" was initially used
in description of angiographic findings in Budd-Chiari syndrome, and it means
presence of very small interwoven veins. This split image (gray scale on right
and color Doppler, shown here in gray scale, on left) shows example of
spiderweb circulation (arrowheads) with Budd-Chiari syndrome. Note
that nonconspicuity of these small-size veins made its visualization really
difficult on gray-scale sonography. On right, only intrahepatic portal vein
(arrow) is evident.
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Fig. 7B —55-year-old man with paroxysmal nocturnal hemoglobinuria
(PNH) who presented with 6-week history of generalized edema and diffuse
abdominal pain. Sonographic study was performed showing that right and left
hepatic veins were obstructed. Pulsed Doppler sonogram obtained 1 year later
illustrates anomalous curvilinear vessel (arrowheads) draining to
inferior vena cava (ivc) replacing obstructed right hepatic vein.
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Fig. 8A —43-year-old man with subacute Budd-Chiari syndrome. Split
image (gray scale on left and color Doppler on right) obtained in intercostal
plane. On gray scale, note curvilinear, fragmented vessels
(arrowheads) that are characteristic for Budd-Chiari syndrome.
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Fig. 8B —43-year-old man with subacute Budd-Chiari syndrome.
Venovenous collaterals are anomalous curvilinear vessels that usually drain to
inferior vena cava, although sometimes inferior vena cava does not show
evidence of connections with other vessels. Color Doppler sonogram in
intercostal plane shows multiple anomalous, curvilinear veins
(arrows) draining to inferior vena cava (arrowheads).
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Collateral Circulation
To decompress liver parenchyma, intrahepatic blood has to find a pathway to
exit the liver. These pathways include the extrahepatic portosystemic
collaterals and the intrahepatic collaterals. Patients in whom Budd-Chiari
syndrome is well controlled with medical treatment develop more intrahepatic
collateral circulation than the patients who require derivative treatment
(TIPS or surgery). This finding reflects the fact that collateral circulation
allows sufficient liver decompression, avoiding symptomatic portal
hypertension [5].
Valla [1] considers
collateral circulation the most sensitive feature for the diagnosis, found in
more than 80% of cases. In our opinion, features such as those shown in
Figures 7A,
7B,
8A, and
8B are characteristic, but the
involvement of hepatic veins to diagnose Budd-Chiari syndrome is also
necessary because similar vessels have been reported in patients with
diaphragmatic hernia, Rendu-Osler-Weber syndrome, and congestive heart failure
[6].
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Fig. 9 —35-year-old woman suffering from chronic Budd-Chiari syndrome
related to myelofibrosis. Color Doppler sonogram, shown here in
black-and-white, displays characteristic collateral vessel in hockey-stick
appearance (arrow). These subcapsular vessels are typical and may
connect with extrahepatic circulation.
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Fig. 10A —36-year-old man with primary thrombocythemia developed
chronic Budd-Chiari syndrome that required transjugular intrahepatic
portosystemic shunt (TIPS) placement. Patient has multiple benign nodules
largely followed without changes. Sonogram shows distal thrombosis of middle
and left hepatic veins (mhv and lhv, respectively) with collateral circulation
within them (arrowhead). Note TIPS (arrows).
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Fig. 10B —36-year-old man with primary thrombocythemia developed
chronic Budd-Chiari syndrome that required transjugular intrahepatic
portosystemic shunt (TIPS) placement. Patient has multiple benign nodules
largely followed without changes. Sonogram in sagittal epigastric line shows
caudate hypertrophy with prominent caudate lobe vein
(arrowheads).
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Fig. 10C —36-year-old man with primary thrombocythemia developed
chronic Budd-Chiari syndrome that required transjugular intrahepatic
portosystemic shunt (TIPS) placement. Patient has multiple benign nodules
largely followed without changes. Color Doppler sonogram, shown here in gray
scale, discloses two iso- and hyperechoic nodules (arrowheads)
surrounded by thin hypoechoic halo. Spectral study shows low resistance
arterial waveform with high velocity.
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Fig. 10D —36-year-old man with primary thrombocythemia developed
chronic Budd-Chiari syndrome that required transjugular intrahepatic
portosystemic shunt (TIPS) placement. Patient has multiple benign nodules
largely followed without changes. Helical CT after IV contrast injection
displays enhancing nodule (arrows) surrounded by low-attenuating area
related to vascular disorders. On helical CT, benign regenerative nodules are
homogeneously hyperattenuating on arterial phase and remain slightly
hyperattenuating on portal vein phase.
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Fig. 11A —39-year-old woman with Budd-Chiari syndrome diagnosed 1 year
ago. Split image showing portal thrombosis. Color Doppler sonogram shows
portal thrombus (thin arrows). Note hepatofugal flow in right portal
vein (arrowhead). Thick arrow points to hepatic artery.
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Fig. 11B —39-year-old woman with Budd-Chiari syndrome diagnosed 1 year
ago. Gray-scale sonogram obtained in transversal epigastric plane shows
evident caudate lobe vein (arrowheads). Note changes in parenchymal
echogenicity (arrows) reflecting vascular disorder. ivc = inferior
vena cava.
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Fig. 12A —32-year-old man with multiple small liver nodules without
changes in 4 years. On color Doppler sonography, regenerative nodules can be
isoechoic or mildly hyperechoic with hypoechoic halo. Poor border definition
is also frequent finding. Most nodules show arterial vascularization (radial
and peripheral) at pulsed Doppler interrogation. Power Doppler sonogram shows
small isoechoic hypervascular nodule (arrows).
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Fig. 12B —32-year-old man with multiple small liver nodules without
changes in 4 years. On color Doppler sonography, regenerative nodules can be
isoechoic or mildly hyperechoic with hypoechoic halo. Poor border definition
is also frequent finding. Most nodules show arterial vascularization (radial
and peripheral) at pulsed Doppler interrogation. Pulsed color Doppler sonogram
shows arterial nature of vessels (arrows).
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Fig. 12C —32-year-old man with multiple small liver nodules without
changes in 4 years. On color Doppler sonography, regenerative nodules can be
isoechoic or mildly hyperechoic with hypoechoic halo. Poor border definition
is also frequent finding. Most nodules show arterial vascularization (radial
and peripheral) at pulsed Doppler interrogation. MR T1-weighted image after
gadolinium injection shows multiple peripheral enhancing nodules
(arrows). On MRI, benign regenerative nodules are hyperintense on
T1-weighted and commonly hyperintense on T2-weighted images (distinctive
finding). There is hypervascularity at dynamic MR study.
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Intrahepatic Venovenous Collaterals
The newly formed vessels can be classified into spiderweb collaterals
(Figs. 7A and
8B), large venovenous
collaterals draining to the inferior vena cava (Figs.
8B and
9A) and subcapsular veins
(Figs. 1B and
3B), and hepatic vein to
hepatic vein shunting [3,
4] (Figs.
4B,
5A,
5B,
5C,
10A,
10B,
10C, and
10D).
Intrahepatic Portacaval Collaterals
Spontaneous direct portacaval shunts perhaps represent the most interesting
hemodynamic circuits we may observe in these patients because they imitate in
a natural way the available treatment options (surgical portosystemic shunts,
TIPS) (Figs. 2C and
2D).
Caudate Lobe Vein
The caudate vein is enlarged in 50% of patients (Figs.
10B and
11B), and visualization of a
caudate vein equal to or larger than 3 mm is a specific sign of Budd-Chiari
syndrome in the absence of heart failure. The caudate lobe is the only segment
that drains directly into the inferior vena cava. This venous system consists
of one proper hepatic vein in most cases. The caudate lobe has a special
relevance in patients with Budd-Chiari syndrome because in many cases the
liver venous drainage is preserved through the caudate vein. Thus, the caudate
vein receives blood not only from the caudate lobe but also from other parts
of the liver, through collateral vessels, leading to an enlargement of both
the vein and the lobe [7].
Other Signs
Multiple benign hepatic nodules (adenomatous hyperplastic nodules, nodular
regenerative hyperplasia, and regenerative nodules) have been observed in
pathologic studies in 60-80% of patients. The routine use of imaging
techniques in the follow-up of patients with Budd-Chiari syndrome has resulted
in increased lesion detection
[8] (Figs.
10C,
10D,
12A,
12B, and
12C). These benign nodules are
thought to be related to a decrease of portal venous flow that leads to
hepatic ischemia with subsequent elevation of hepatocellular growth factors,
stimulating new arterial growth. These nodules share the feature of
hypervascularity with hepatocellular carcinoma, so it is not possible to
differentiate between them by using imaging techniques. Although regenerative
nodules may be hypointense on T2-weighted images, overlapping exists between
the two diseases. In general, patients with Budd-Chiari syndrome who have
nodules with a normal level of 
-fetoprotein are followed using imaging
techniques, and the lack of growth is synonymous with benignity. Biopsy is
advised in doubtful cases (e.g., nodule enlargement or chronic hepatitis B or
C).
Nonspecific morphologic changes such as liver enlargement and
hypoechogenicity of the segments drained by the obstructed hepatic vein or
veins are observed in the acute phase. In the chronic stage, persistent
hepatic outflow obstruction results in fibrosis, and the affected areas shrink
and show parenchymal heterogeneity similar to that of liver cirrhosis.
The caudate lobe is enlarged in most patients (80%)
[1,
2], explained by the
preservation of the caudate lobe vein draining to the inferior vena cava
[3,
4,
7]. In some cases this
enlargement can compress the inferior vena cava, complicating the liver
hemodynamics.
Portal vein thrombosis is associated with a poor prognosis and reported in
10-20% of patients [1]. The
presence of hepatofugal flow in the main portal vein reflects a significantly
increased intrahepatic pressure (Fig.
11A). Another phenomenon is
the finding of hepatofugal flow in the right portal vein branch but with a
hepatopetal flow in the portal vein trunk. In this situation, the intrahepatic
collaterals connect with the right portal branch, and the blood drains to the
left portal vein, leaving the liver through a recanalized umbilical vein. The
hepatofugal flow, the recanalized umbilical vein, and the ascites are signs
related to a severe portal hypertension.
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Abstract
Introduction
